Suggesting that Cytomegalovirus Infection Contributes to Metabolic Syndrome

Suggesting that Cytomegalovirus Infection Contributes to Metabolic Syndrome

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Metabolic syndrome is the precursor to type 2 diabetes, and is caused by the presence of excess visceral fat tissue. Age is a factor, however, in that people become more susceptible to the harmful consequences of being overweight in later life. Why is this the case? Recent evidence points towards the creation of additional lingering senescent cells as an important mechanism linking fat tissue to chronic inflammation and disruption of metabolism. Cellular senescence is an age-related mechanism.

cytomegalovirus (CMV) infection. CMV is very prevalent, and the consensus on its effects is that its presence is an important contribution to the decline of the immune system with advancing age. Too many immune cells become specialized to tackling CMV, leaving too few for other tasks. In the context in which the supply of new immune cells is greatly diminished, due to loss of thymic tissue, and declining activity of hematopoietic stem cells, this is a big problem.

Cytomegalovirus (CMV) is a ubiquitous herpesvirus infecting most of the world’s population. CMV has been rigorously investigated for its impact on lifelong immunity and potential complications arising from lifelong infection. A rigorous adaptive immune response mounts during progression of CMV infection from acute to latent states. CD8 T cells, in large part, drive this response and have very clearly been demonstrated to take up residence in the salivary gland and lungs of infected mice during latency. However, the role of tissue resident CD8 T cells as an ongoing defense mechanism against CMV has not been studied in other anatomical locations.

Therefore, we sought to identify additional locations of anti-CMV T cell residency and the physiological consequences of such a response. Through RT-qPCR we found that mouse CMV (mCMV) infected the visceral adipose tissue and that this resulted in an expansion of leukocytes in situ. We further found, through flow cytometry, that adipose tissue became enriched in cytotoxic CD8 T cells that are specific for mCMV antigens from day 7 post infection through the lifespan of an infected animal and that carry markers of tissue residence. Furthermore, we found that inflammatory cytokines are elevated alongside the expansion of CD8 T cells. Finally, we show a correlation between the inflammatory state of adipose tissue in response to mCMV infection and the development of hyperglycemia in mice.

Overall, this study identifies adipose tissue as a location of viral infection leading to a sustained and lifelong adaptive immune response mediated by CD8 T cells that correlates with hyperglycemia. This data potentially provides a mechanistic link between metabolic syndrome and chronic infection.


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